コーパス検索結果 (1語後でソート)
通し番号をクリックするとPubMedの該当ページを表示します
1 in the presence of NADPH by cell-free assay (cytochrome c).
2 f hemes through deprotonated histidine (e.g. Cytochrome c).
3 itin, eglin c, ribonuclease A, lysozyme, and cytochrome c).
4 a number of heme protein systems, including cytochromes c'.
5 state abundances of both c-type cytochromes, cytochrome c (1) and cytochrome c The observed reduction
9 with decreasing protein molecular mass: for cytochrome c (12.3 kDa) and lysozyme (14.3 kDa) a detect
10 (PNA) can be used to control the assembly of cytochrome c (12.5 kDa, pI 10.5) and azurin (13.9 kDa, p
11 exhibited significant rates of reduction of cytochrome c (160 min(-1), largely superoxide dismutase-
12 efficiently as wild type MSR but the rate of cytochrome c, 2,6-dichloroindophenol, and menadione redu
14 SI centers that are prebound by plastocyanin/cytochrome c (6) in darkness (about 60% in both cyanobac
15 isotopes at the fundamental distribution of cytochrome c(+8) (m/z approximately 1549) were nearly ba
16 by DESI-MS, were 100% for melittin, 100% for cytochrome c, 90% for myoglobin, and 65% for bovine seru
17 properties are reminiscent of the A-state of cytochrome c, a compact denatured form found under acidi
18 fic ablation of the proapoptotic function of cytochrome c, a key regulator of mitochondria-mediated a
21 the presence of reactive oxygen species and cytochrome c, a proapoptotic peroxidase that is released
22 lso propose an orientation of membrane-bound cytochrome c, a protein for which the membrane orientati
24 om proteins; a deamidated tryptic peptide of cytochrome c, a tryptic peptide from unfolded and deamid
25 mitochondrial membrane potential, release of cytochrome c, activation of Bax and Bak, and processing
26 Ad-MMP-9 infection induced the release of cytochrome c, activation of caspase-9 and -3, and cleava
27 mitochondrial permeability shift, release of cytochrome c, activation of caspases, and subsequent fra
28 3 and 9) and in the mitochondrial (cytosolic cytochrome C, AIF, Mcl-1, Bcl-2, Bcl-xl, Bax, Bad, and p
29 res contained four basic proteins (lysozyme, cytochrome c, alpha-chymotrypsinogen A, and ribonuclease
32 (flavoprotein, succinate dehydrogenase, and cytochrome c) and the synthesis and activity of key deni
33 depolarizes mitochondria membranes, releases cytochrome c, and activates caspases-9 and -3 and death
34 hondrial membrane depolarization, release of cytochrome c, and activation of both intrinsic and extri
37 chondrial proteins, release of the apoptogen cytochrome c, and activation of executioner caspase-3 we
38 islets was strongly correlated with reduced cytochrome c, and agents that acutely and specifically r
39 ized HAzPC associated with mitochondria, and cytochrome c, and apoptosis-inducing factor escaped from
41 formed in ESI for three proteins (ubiquitin, cytochrome c, and carbonic anhydrase II) were investigat
43 ell death with immunostaining for annexin V, cytochrome C, and caspases 3 and 9 pointing to induction
44 Bax expression, a disturbed distribution of cytochrome c, and cleaved caspase-3 positive staining in
45 e purification of the engineered peroxidase, cytochrome c, and covalent complex, along with activity
47 aspase-8, deficient release of mitochondrial cytochrome c, and delayed activation of both caspase-9 a
48 duced unfolding of SNase, from acid-unfolded cytochrome c, and from folding of Azoarcus ribozyme.
49 in blocking apoptosis by reduction of ferric cytochrome c, and gentle tuning of NO concentration in t
52 enzymatic activity and immunoreactivity for cytochrome c, and identical functional properties shared
53 ious Mossbauer investigations on a bacterial cytochrome c, and is not reproduced by the simulations.
54 of the mass spectral response for myoglobin, cytochrome c, and lysozyme is presented for laser electr
57 as well as mitochondrial release of AIF and cytochrome c, and subsequent activation of caspase-9 in
58 on of the effector caspase-9, independent of cytochrome c, and subsequently the processing of the exe
59 f caspases, apoptogenic mitochondrial factor cytochrome c, and the Bcl-2 family proteins in DR6-induc
60 R) in portal blood, the release of cytosolic cytochrome c, and the cleaved caspase 9 expression in in
61 cular, appeared to be restricted to nitrated cytochrome c, and thus, no association of non-nitrated c
62 elease, lipid peroxidation, translocation of cytochrome c, and TUNEL labeling in the ischemic cortex.
64 esults constitute the molecular mechanism of cytochrome c- and dATP-mediated activation of Apaf-1.
65 2 positions (C(18:2)/C(18:2)), formed in the cytochrome c- and H(2)O(2)-driven enzymatic oxidation re
66 acid-binding protein, myoglobin and somatic cytochrome-C) and others (creatine kinase M, malate dehy
67 e myocardial levels of lipid hydroperoxides, cytochrome-c, and mitochondrial aconitase activity were
68 ns c-Jun N-terminal kinase 3, caspase 3, and cytochrome C, Annexin V staining, RNA degradation, and o
69 tryptophans in three well-studied proteins, cytochrome c, apomyoglobin, and lysozyme, as a function
70 her a caspase-dependent mechanism, involving cytochrome c, apoptosis protease-activating factor-1 (Ap
71 avage; and Bcl-2 phosphorylation, as well as cytochrome c, apoptosis-inducing factor (AIF), and endon
73 apparent K(d),of ~15.8 muM and competes with cytochrome c (apparent K(d) of ~1.31 muM) for binding to
74 D ( approximately 16% decrease, males only), cytochrome C ( approximately 19% decrease, females only)
75 ase of intermembrane space proteins, such as cytochrome c, are early events during intrinsic (mitocho
79 a picosecond timescale for the heme protein, cytochrome c, as a function of oxidation and hydration,
80 gment-elevation AMI patients with detectable cytochrome c, as compared with those with nondetectable
81 s approach to the absolute quantification of cytochrome C (as target compound) in a commercial protei
82 terial heme protein Alcaligenes xylosoxidans cytochrome c' (AXCP) forms a novel five-coordinate heme-
84 % (w/v) bovine serum albumin and 0.01% (w/v) cytochrome C (both are proteins), and 0.002% (w/v) human
85 ation and identification of proteins such as cytochrome c, bovine serum albumin, and high-molecular w
86 brane pores large enough to release not only cytochrome c, but also allophycocyanine, a protein of 10
87 erobic electron acceptors include oxygen and cytochrome c, but an acceptor that can function under an
88 electrons coming from NADH and ubiquinol to cytochrome c, but it is also capable of producing signif
89 sequent release of the mitochondrial protein cytochrome c, but the second mitochondrion-derived activ
91 a result, during steady-state turnover with cytochrome c, calmodulin now deactivates the enzyme and
92 induced mitochondrial trafficking of Bax and cytochrome c, caspase-3 activation, and oxidative stress
93 he product of the enzymatic reaction reduces cytochrome c, causing an increase in absorbance at 550 n
97 s to the periplasmic enzymes that reduce apo-cytochrome c (CcsX) or repair oxidative protein damages
98 H2O2-dependent apoptosis in mouse embryonic cytochrome c(+/+) cells than in cytochrome c(-/-) cells.
100 ria differed primarily at a Raman biomarker, cytochrome c, corresponding to a bacteroid-specific term
101 ns (i.e., myoglobin, carbonic anhydrase, and cytochrome c) could be analyzed by SEC-ESI-MS using diff
102 arkers of WAT mitochondrial protein content (cytochrome c, COXIV-subunit I, and citrate synthase acti
105 and the nuclear-encoded subunits of COX and cytochrome c (CYC), we hypothesized that some codons in
106 lus fumigatus alternative oxidase (aoxA) and cytochrome C (cycA) null mutants and assessed their abil
107 rving as respiratory electron shuttle, ferri-cytochrome c (cyt c) acts as a peroxidase; i.e., it cata
108 ns and ER stress as shown by increased HSP60/Cytochrome C (Cyt C) and CHOP-ATF3 levels respectively.
109 d, catalytic circuit based on photosystem I, cytochrome c (cyt c) and human sulfite oxidase (hSOX).
110 An axial S(Met) bond is also present in cytochrome c (cyt c) and is generally thought to increas
111 proach with three variants of a heme protein cytochrome c (cyt c) and show that the method yields a w
112 tive stress sensor contains the heme protein cytochrome c (cyt c) as sensing element whose spectral r
114 tivation of peroxidase catalytic function of cytochrome c (cyt c) by anionic lipids is associated wit
115 y to investigate the early folding states of Cytochrome c (cyt c) by monitoring the distance between
116 ted for the first time that the heme protein cytochrome c (Cyt c) can enter the interior of a MOF des
118 cribe advancements in sensing technology for cytochrome c (cyt c) detection, at point-of-care (POC) a
121 denatured states and the native structure of cytochrome c (Cyt c) from Saccharomyces cerevisiae.
122 activation is accompanied by the release of cytochrome c (cyt c) from the intermembrane gap and subs
128 competent peroxidase form of pentacoordinate cytochrome c (cyt c) in a complex with a mitochondria-sp
129 vine serum albumin (BSA), lysozyme (lyz) and cytochrome c (cyt c) in singular and competitive manner
130 of Thr78Cys/Lys79Gly/Met80X mutants of yeast cytochrome c (cyt c) in which Cys78 becomes one of the a
141 arly mitochondria-specific cardiolipin (CL), cytochrome c (cyt c) loses its tertiary structure and it
142 cytochrome c synthase (HCCS) is required for cytochrome c (cyt c) maturation and therefore respiratio
145 tion of cardiolipin (CL) by its complex with cytochrome c (cyt c) plays a crucial role in triggering
148 has been suggested that the alkaline form of cytochrome c (cyt c) regulates function of this protein
149 tic stress induces apoptosis, which involves cytochrome c (Cyt c) release from mitochondria and subse
152 s of the spontaneous reversible unfolding of Cytochrome c (Cyt c) under native conditions have led to
159 interaction of the simple, globular protein cytochrome C (Cyt C) with MPMN surfaces using experiment
160 rochemical immunosensor for the detection of cytochrome c (cyt c), a heme containing metalloprotein u
165 nsfer reorganization free energy (lambda) of cytochrome c (Cyt) in electrostatic complexes that mimic
166 the adsorption behavior of the redox protein cytochrome c (Cyt-C) onto different interfaces, namely,
169 hieved using redox cofactors namely oxidized cytochrome-c (Cyt-c) and Co-enzyme-Q (Co-Q) immobilized
172 of mitochondrial permeability and release of cytochrome c (CytC) and apoptosis-inducing factor (AIF)
173 as an oligopeptide stopper, we have employed cytochrome C (CytC) as a protein stopper to produce the
179 r the directed immobilization of horse heart cytochrome c (cytc) on gold electrode surfaces to achiev
180 tion (MOMP) via BAK and BAX oligomerization, cytochrome c (cytc) release, and caspase activation are
182 -phycoerythrin (R-PE) and positively charged cytochrome c (CYTC) within the same DFGF apparatus is sh
183 te ETp across the electron-mediating protein cytochrome c (CytC), measured in a monolayer configurati
186 rate synthase), and the expression levels of cytochrome c, cytochrome c oxidase subunit 1, and mitoch
187 + H2O) with electrons donated by periplasmic cytochrome c (cytochrome c-dependent NO reductase; cNOR)
188 hibitor, prevented the increase in cytosolic cytochrome c, decreased caspase-3 activation, and partia
189 polarization of mitochondria, and release of cytochrome c, demonstrating its important role as an ant
191 es for all three monomeric proteins, and for cytochrome c, dimers of significant intensity are also o
192 in an observed sequence coverage of 79% for cytochrome C (eight peptides), 47% for beta-lactoglobuli
193 hampers mitochondrial respiration, releases cytochrome c, elevates mitochondrial lipid peroxidation,
194 ectron transfer-triggered folding of reduced cytochrome c, far-UV time-resolved circular dichroism (T
195 65 mM SDS to induce the MG state in oxidized cytochrome c, folding of redcyt c was triggered with fas
197 -coordinate heme-nitrosyl complex (5c-NO) of cytochrome c' from Alcaligenes xylosoxidans (AXCP) in wh
198 either heme face exists, as in the microbial cytochrome c' from Alcaligenes xylosoxidans (AxCYTcp), w
202 re reveals a core that is typical of class I cytochromes c, having alpha-helices folded into a compac
204 -Volmer quenching constants (Ksv) for hemin, cytochrome c, hemoglobin, and myoglobin were 5.6x10(7),
205 ta defensin 1, truncated human lymphotactin, Cytochrome C, holo hemoglobin-alpha, ovalbumin, human tr
206 ged: the first was to maintain the KD of the cytochrome c' in the 1 microM range, and the second was
208 n conformations of a small globular protein, cytochrome c, in the presence of guanidine hydrochloride
209 d had greater amounts of cytosolic mtDNA and cytochrome c, increased apoptosis, and more IL-1beta sec
210 eased activation of caspase-3 and release of cytochrome c, indicating that a mitochondrial pathway wa
212 wnstream of the mitochondria, with cytosolic cytochrome c, kills brain tumor cells but not normal bra
213 nents abolishes the ability of cells to form cytochrome c, leading in the case of Rhodobacter capsula
215 mP in a complex with its substrate, L. major cytochrome c (LmCytc) to 1.84 A, and compared the struct
218 ion to peptides, gas-phase HDX of ubiquitin, cytochrome c, lysozyme, and apomyoglobin were examined.
220 s circumvented by deleting the gene encoding cytochrome c (M) (CytM), a cryptic c-type heme protein w
222 (NANOG, MYOD), antibodies, native proteins (cytochrome C), magnetic nanoparticles (MNPs), and nuclei
224 horylation and fatty acid oxidation, such as cytochrome c, medium-chain acyl-CoA dehydrogenase, and a
226 dione or benzoquinone and weak activity with cytochrome c, molecular oxygen, and 5,5'-dithio-bis-2-ni
227 releases of a small protein (8 muL of 5 muM cytochrome-c, molecular mass ~12 kDa) and exhibits ~1 mi
228 The spectra for smaller proteins (ubiquitin, cytochrome c, myoglobin) again resemble those at AP, pro
232 A mixture containing four model proteins (cytochrome c, myoglobin, bovine serum albumin (BSA), and
234 usion rates of 6 Hz are used for analysis of cytochrome c, on a DTIMS Q-TOF similar rates were obtain
235 the transport of electrons from ubiquinol to cytochrome c (or alternate physiological acceptors), yet
236 V(max) of each in four assays: reduction of cytochrome c, oxidation of NADPH, 17alpha-hydroxylase ac
239 tra of the B-bands of bovine and horse heart cytochrome c (pH 7.0) exhibit a pronounced couplet that
240 , Apaf-1, procaspase-9, procaspase-3, Hsp70, cytochrome c, PHAPI, CAS, and regulatory compounds to mi
241 -to-Bcl-2 ratio (R(2) = 0.83) and release of cytochrome c (R(2) = 0.92), but preceded in time the cas
245 d to be 350 and 25 mg/ml for rusticyanin and cytochrome c, respectively; cytochrome a was present as
248 the refolding of Rhodopseudomonas palustris cytochrome c' reveals dramatic differences between two v
249 -cytochrome c and Rhodopseudomonas palustris cytochrome c', shows that foldable sequences deviate sig
250 anied by mitochondrial injury and release of cytochrome c, Smac, and AIF into the cytosol and caspase
253 pathological changes and increased levels of cytochrome c, Smac/DIABLO and AIF in the cytosol while t
254 ay, leading to increased cytosolic levels of cytochrome c, Smac/Diablo and Omi/HtrA2, and activation
255 embrane potential, attenuated the release of cytochrome c, Smac/DIABLO, and apoptosis inducing factor
256 mitochondrial depolarization and release of cytochrome c, Smac/DIABLO, and apoptosis-inducing factor
257 The protein expressions of mitochondrial cytochrome c, stromal cell-derived factor-1, C-X-C chemo
258 n transferase activity with equine and yeast cytochrome c, suggesting a conservation of the enzymatic
259 Apaf-1 and rendered the cells insensitive to cytochrome c, suggesting a potential role for Rsk signal
260 th released the apoptogenic factors Smac and cytochrome c, suggesting that they are primed for cell d
261 o affect the buried hydrogen bond network of cytochrome c, suggesting that this network is an importa
262 While the N-terminal domain is a class I cytochrome c, the C-terminal domain shows no similarity
263 ee proteins of increasing intrinsic disorder-cytochrome c, the tumor suppressor protein p53 DNA bindi
264 The surprising finding is that, unlike for cytochrome c, there is an observable folding intermediat
266 imilar to the previously reported results on cytochrome c, these fragment ions form near residues kno
267 that reduced DSD-Fdm transfers electrons to cytochrome c, thus generating the reduced cyt c stoichio
268 r binding affinity of rebaudioside A towards cytochrome c, thus supporting their host-guest relations
270 id hydrolysis to degrade a standard protein, cytochrome c, to produce many di/tripeptides with known
272 t with MPH (10mg/kg) decreased caspase-3 and cytochrome c; treatment with MPH (2 and 10mg/kg) increas
273 abilities are demonstrated for ubiquitin and cytochrome c, two common model proteins for structure an
274 obilities of single multiply charged ions of cytochrome c, ubiquitin, myoglobin, and bovine serum alb
276 ein SERS spectra of a layer of test protein, Cytochrome-c, using a custom-made Otto-Raman spectroscop
277 reactivity of the reduced FMN domain toward cytochrome c; (v) response to calmodulin binding; and (v
278 of model proteins in aqueous media, such as cytochrome c, was also examined, yielding spectra with a
280 functionally relevant structural changes in cytochrome c, we measured the absorption and electronic
281 ins (transferrin, myoglobin, hemoglobin, and cytochrome c) were separated by high-performance liquid
282 the SH3 domain, dihydrofolate reductase, and cytochrome c, where the transparent window vibrational p
283 calmodulin (CaM)-free and CaM-bound nNOS to cytochrome c, whereas hinge lengthening relieved repress
284 ngly abolish formation of both holo-CcmE and cytochrome c, whereas previously reported point mutation
285 ants, such as bovine cytochrome c and equine cytochrome c, which differ by only three amino acids.
286 MOM permeabilization, causing the release of cytochrome c, which effectively commits the cell to die.
288 eabilization (MOMP), allowing the release of cytochrome c, which interacts with Apaf-1 to trigger cas
289 tion and inhibits the peroxidase activity of cytochrome c, which is involved in its release from mito
290 2)S also reduces CcO's biological reductant, cytochrome c, which normally derives its reducing equiva
292 he dissociated heme to the protein moiety in cytochrome c, which we assign to the presence of covalen
293 hondrial damage and translocation of Bax and cytochrome c, which were then followed by caspase-3 acti
294 n aberrant activation of a testis isoform of cytochrome c, which, albeit expressed at low levels, was
295 different proteins (Trp-cage, myoglobin, and cytochrome c) with folding time constants that differ by
296 1 functioned as a translational repressor of cytochrome c, with interventions to silence TIA-1 dramat
297 roxidase (ZnCcP) in complex with yeast iso-1-cytochrome c (yCc) diffract to higher resolution (1.7 A)
298 ection values of the charge states of equine cytochrome c (z = 9-16), and values are in good agreemen
299 e demonstrate that Zn(II) porphyrin in Zn(II)cytochrome c (Zn cyt c) is a fluorescence resonance ener
300 phyrin (ZnP) chromophore in zinc-substituted cytochrome c (Zn-cyt c) and an Alexa Fluor dye attached